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Centre d’Immunologie Pierre Fabre, Saint-Julien en Genevois, France;
Pharmacie Centrale, Centre Hospitalier, Hazebrouck, France; and
Institut National de la Santé et de la Recherche Médicale Unité 416, Institut Pasteur, Lille, France
Mast cells and immature dendritic cells (DC) are in close contact
in peripheral tissues. Upon activation, mast cells release histamine, a
mediator involved in the immediate hypersensitivity reaction. We
therefore tested whether histamine could affect human DC activation and
maturation. Histamine induces CD86 expression on immature DC in a
dose-dependent (significant at 10-7 M) and transient
manner (maximal after 24-h stimulation). Histamine also transiently
up-regulates the expression of the costimulatory and accessory
molecules, CD40, CD49d, CD54, CD80, and MHC class II. As a consequence,
immature DC exposed for 24 h to histamine stimulate memory T cells
more efficiently than untreated DC. In addition, histamine induces a
potent production of IL-6, IL-8, monocyte chemoattractant
protein 1, and macrophage-inflammatory protein 1
by immature
DC and also up-regulates IL-1
, RANTES, and macrophage-inflammatory
protein 1 but not TNF- and IL-12 mRNA expression. Histamine
activates immature DC through both the H1 and H2 receptors. However,
histamine-treated DC do not have a phenotype of fully mature cells, as
they do neither show significant changes in the expression of the
chemokine receptors, CCR5, CCR7 and CXC chemokine receptor 4, nor
expression of CD83 de novo. These data demonstrate that histamine
activates immature DC and induces chemokine production, thereby
suggesting that histamine, via stimulation of resident DC, may
participate locally in T cell stimulation and in the late inflammatory
reaction associated with allergic disorders.
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